SlideShare ist ein Scribd-Unternehmen logo
1 von 59
ENCEPHALOPATHY: TYPES, SYMPTOMS,
CAUSES, STAGES & TREATMENT
 Derived from Greek word “enkephalos”- meaning brain.
 “Pathos” meaning is disease.
 The term “encephalopathy” is defined as altered mental status as a result of a
diffuse disturbance of brain function.
 It represents a brain state in which normal functioning of the brain is disturbed
temporarily or permanently.
 Any clinical condition that causes impairment in consciousness usually
accompanied by diffuse EEG abnormalities
Types & Causes of encephalopathy
 Reversible
 metabolic encephalopathy,
 Hashimoto’s encephalopathy,
 hepatic encephalopathy,
 infectious of the brain,
 brain tumours,
 toxic encephalopathy,
 nonconvulsive status epilepticus
 Irreversible
chronic traumatic encephalopathy
Hypoxic-ischemic encephalopathy
Causes of encephalopathy
• Encephalopathy results main from,
• Metabolic derangements (Na, K, Ca)
• Toxins (exposure to toxic substances, e.g lithium paints, industrial
• chemicals)
• infectious (bacteria (TB) viruses, parasites, or prions),
• Hepatic (liver failure or liver cancer)
• Inflammations (Systemic Lupus Erythropetosis, sarcoidosis (soft
• tissues diseases)
• Drug Induced (Over dozage of the drug)
• Demyelinating (e.g MS)
• Degenerative processes (Alzheimer disease, Parkinson's disease)
• Anoxic encephalopathy (lack of oxygen to the brain, including
traumatic
• causes)
• Hereditary encephalopathies (leucodystrophy white matter)
SYMPTOMS
 Common symptoms
• confusion
• memory loss
• personality changes
• troubling in thinking or
focusing
 Less common symptoms
• trouble in speaking
• muscle weakness or twitches
• tremors
• seizures
• sleepiness
Hepatic encephalopathy
Definition: Hepatic encephalopathy is a reversible neuropsychiatric
state that complicates severe liver disease.
• Encephalopathy associated with Cirrhosis and portal hypertension
• Encephalopathy associated with portal systemic Bypass without
hepatocellular disease
• Encephalopathy associated with Acute liver failure
Clinical features
1. Disturbed consciousness:
Sleep disturbance (change of sleep pattern to hypersomnia , or
drowsiness ) Confusion including delirium Unconscious
2. Abnormal behavior
3. Intellectual deterioration (cognition)
4. Abnormal nerve reflexes Flapping tremor (asterixis)
Clinical grading
• Stage 1: Abnormal sleep, Abnormal behavior (mood change e.g.
euphoria/depression, strange behavior ) Altered cognition (
decreased attention and calculation ability) Flapping tremor (+/-) EEG
(+/-)
• Stage 2: Lethargic, Inappropriate behavior Disorientation and
memory decreased Flapping tremor (+), abnormal nerve
reflexes(ataxia) EEG (+) Clinical grading
• Stage 3: Somnolence but can be aroused, marked confusion
(delirium) Flapping tremor (+), abnormal nerve reflexes EEG (+)
• Stage 4: unconsciousness (can not be aroused) abnormal to loss of
reflexes
Investigation
• 1. Blood ammonia
• 2.Electroencephalogram
• 3. Evoked potentials
• 4. Psychometric tests
Treatment
. Identification & correction of the precipitating cause:
• Precipitating factors
• Drugs!
• Electrolyte imbalance – hypokalemia/metabolic alkalosis (diuretics,
vomiting, diarrhea, infusion)
• GI Bleeding Infection
• Constipation
• Large protein meal
Cont.
 Intervention to reduce the production & absorption of gut-derived
ammonia & other toxins:
• 1) Diet: reduce and modify dietary protein and maintain Calorie intake
• 2) Enemas (mild acid) and/or purgation
• 3) Lactulose or lactitol
• 4) Inhibition of gut bacteria: Antibiotics: neomycin(oral), metronidazone?
• 5) Modification of colonic flora: probiotics?
Modify colonic flora, resulting in displacement of urease-containing bacteria
with lactobacillus Cathartic effect
Lower the colonic pH, resulting in the formation of non-absorbable NH4
from NH3 in the colon
Metabolic encephalopathy
Pathophysiology:
• Mainly it depends on the cause However regardless the etiology the
main mechanism is due to disruption of arousal and attention centers
in the brain (ARAS).
• Another mechanism including compression or injury for areas critical
for memory ,attention and executive functions .
• Abnormalities in neurotransmitters such as ( (Ach , serotonin, GABA
,dopamine, tryptophan ,cytokines ) also affect these connections.
Uremic encephalopathy
Pathology :
• Decrease clearance of osmotically active toxins
• Proinflammatory state lead to BBB breakage
• Electrolytes abnormailites
• Seziures and myoclonus
• Dysequilibrium syndrome
• Dialysis dementia
• Cerebral atrophy
symptoms:
• Seizures and myoclonus
• Permanent memory loss
• Dysarthria
• Facial grimacing
• Myoclonus
• Mood and personality changes
• Confusion
• Headache
• Nausea and vomiting
• Tremors
Prognosis:
• Metabolic encephalopathy is common in the ICU setting
• the brain dysfunction that occurs with metabolic encephalopathy was
thought to be completely reversible
• critically ill patients with metabolic encephalopathy are often left
with long-term neurocognitive deficits.
• Persistent neurologic and psychiatric deficits occur in up to 32% of
medical ICU survivors
Management:
• Any of abnormal movement presented in renal patient should be
evaluated by EEG confirm diagnosis of myoclonus
• • Phenytoin used as AEDs in uremic patient to control sezuires but it
worse myoclonus
• • Best choice for myoclonus is tiratam &valporic acid
HASHIMOTO ENCEPHALOPATHY
• Defined by the detection of thyroid peroxidase (TPO) antibodies in
patients with acute or subacute encephalitis that responds to
steroids.
• “Encephalopathy associated with autoimmune thyroid disease” is
considered more accurate- due to normal thyroid function.
• Very vague symptoms- unclear course
Clinical features: non specific
• Stroke-like symptoms
• Tremor, myoclonus
• Transient aphasia
• Sleep and behaviour abnormalities
• Hallucinations, seizures and ataxia.
Diagnosis:
• clinical triad of neuropsychiatric symptoms, detection of antimicrosomal or
antithyroglobulin antibodies, and exclusion of other causes.
• antithyroid peroxidase, antithyroglobulin,
• lesser extent thyroid-stimulating hormone receptor
• blocking antibodies.
• α-enolase
• CSF show moderately elevated protein, may be positive for anti thyroid Ab, OCB
seen
• EEG: slowing, triphasic waves, epileptiform discharges.
• MRI usually normal, occasionally non-specific sub cortical white matter T2 signal
changes.
• Thyroid status may be normal.
Treatment:
• Initial treatment is usually with oral prednisone (50– 150 mg/day) or
high-dose IV methylprednisolone (1 g/day) for 3–7 days. Thyroid
hormone treatment is also included if required.
• Failure of some patients to respond to this first line treatment has
produced a variety of alternative treatments including azathioprine,
cyclophosphamide, chloroquine, methotrexate, periodic intravenous
immunoglobulin and plasma exchange.
• Seizures, if present, are controlled with typical antiepileptic agents.
• Recurrence – continued steroids, IVIG, other immunomodulatory
drugs.
NMDA ENCEPHALOPATHY
• Leading cause of autoimmune encephalitis in children and
adolescents.
• Age- frequently 2– 40 years, 80% Female
• Stages :
• Stage1 – prodromal phase
• Stage 2 – psychiatric and behavioral problems
• Stage 3 – Decreased level of consciousness
• Behavioral changes included new-onset temper tantrums, agitation,
aggression, and changes in mood or personality
Clinical features:
• Behavioural disturbance,Psychosis
• Catatonia
• Seizures
• Movement disorders including orolingual dyskinesias and stereotypic
movement.
• Dysautonomia.
• Ovarian teratoma is associated in up to 50% of the cases
Diagnosis
• CSF : -lymphocytic pleocytosis,
-elevated protein levels
-oligoclonal bands
• EEG – extreme delta brush
• MRI demonstrate medial temporal lobe attenuated inversion recovery
high signal or focal areas of hyperintensity in the frontal or parietal
cortex
• fluorodeoxyglucose positron emission tomography (FDG-PET) scan
show cortical hypermetabolism in acute stages, and hypometabolism
in more subacute stages of the illness.
Treatment
• first line of immunotherapies including corticosteroids, intravenous
immunoglobulin, or plasma exchange
• Rituximab and cyclophosphamide, alone or combined, are often
effective in adults
• Approximately 80% of patients have substantial or full recovery.
Septic encephalopathy
• The term "septic encephalopathy" :
• acute confusional episodes or other significant cognitive
abnormalities that develop during sepsis
• as an entity that cannot be explained by hepatic or renal dysfunction,
hypotension, or hypoxia
• Occur in a range of 8–70% of septic patients
• May as an early sign of sepsis
• Imply poor prognosis , higher mortality
Etiology and pathopysiology
• Most likely multifactorial
• Underlying mechanisms only been defined in parts
• Disseminated cerebral microabscesses
-infecting organisms and/or their toxins do not directly cause
encephalopathy.
• Systemic inflammation resulting from infection or other causes
action of inflammatory mediators on the brain , cytotoxic response of
brain cells
Cont.
• Free radicals
• damage RBC and limit O2 delivery to brain
• Inflammatory mediators
• impair mitochondrial function and O2 extraction by the brain
destroy BBB
• perimicrovessel edema
• disruption of astrocyte endfeet
• aromatic a.a enter brain parenchyma and disturb NT
• Ultimately, extensive neuronal injury
Diagnosis
No specific test available
Electroencephalopathy
• Most sensitive diagnostic tool
• Normal, diffuse slowing,excessive theta,predominantly delta,triphasic waves, and suppression or burst
suppression.
• Evaluating depressed consciousness in critically ill p`ts
• (1) Receiving sedative and narcotic drugs
• (2) Head injury , intracranial event e.g. cerebrovascular causes
• (3) Metabolic derangements :
• Sugar , electrolytes (Na ,Ca) , acid-base balance (acidemia , hypercapnia), oxygenation (hypoxia
,hypotention) , hepatic encephalopathy ,uremic encephalopathy , septic encephalopathy , alcohol or drug
• TREATMENT:
According to cause of septicemia
If hypotension start inotropic supports
Question.
• A 21-year-old primigravida with gestation age of 33weeks whose first
and second trimester gestation was uneventful with no history of
hypertension and epilepsy before and during pregnancy. She
developed sudden onset of headache, giddiness, vomiting, and
convulsions. Her blood pressure was 142/94 mmHg. Next day, the
patient was taken into C section for fetal distress. On 2nd day of
postcaesarean section she developed loss of vision, headache, and
vomiting. Her blood pressure was 140/114 mmHg.
PRES
• Posterior Reversible Encephalopathy Syndrome.
• Variety of symptoms – headache, altered mental status, visual
disturbances, and seizures.
• Hypertension, Pre-eclampsia/eclampsia, immunosuppression, sepsis,
chemotherapy, collagen vascular disease, and renal failure.
Question.
• A 36-year-old real estate agent was in the first trimester of her first
pregnancy when she awoke with diplopia. She had not been well for
several days, feeling lethargic, off-balance and slightly disoriented;
symptoms that she attributed to severe morning sickness during the
previous eight weeks. She was not taking any medications and had
been previously healthy. Exam revealed bilateral ptosis, limitation of
gaze in all directions, slow upward saccades, upbeat nystagmus and
mild ataxia.
• Wernicke’s encephalopathy –
• triad of ophthalmoplegia, ataxia, and confusion. O
• Triad – minority of cases. O
• Ocular findings – earliest and most constant. O
• About 30% have isolated or predominant mental status changes
ranging from confusion to frank coma. O
• Sometimes – sudden onset.
Mangement
• Low serum erythrocyte transketolase – days to obtain.
• Treat on suspicion.
• MRI – specific (93%) but sensitivity is low.
CNS infections/Para-infection
Clinical features:
• Fever , headache
• Meningism
• Focal neurological deficits
• Seizures
• Primary source of infection
• Pneumonia (bacteria, mycoplasma, TB), purpuric rash
(meningococcemia), mucosal herpetic lesions, cyanotic heart dis.
(brain abscess)
Investigations:
• CBC, CRP, ESR
• Blood culture
• Viral study (blood, throat, urine, stool)
• TB work-up
• CSF: ME, sugar, protein, C&S, virology, TB, fungus
Tumour /CNS Malignancy
• Suggestive features
• Signs & symptoms of raised ICP
• Focal neurological deficit
• Seizures
• Extra-cranial primary malignancy
• Neuro-imaging: 1 st line investigation
Toxic encephalopathy
• Toxic encephalopathy, also known as toxic metabolic encephalopathy,
is a degenerative neurologic disorder caused by exposure to toxic
substances.
• It can be an acute or a chronic disorder.
• Toxic encephalopathy can be caused by various chemicals, some of
which are commonly used in everyday life (paints, industrial
chemicals, and certain metals).
EEG in encephalopathy
In general,
• the most prominent feature of the EEG record in encephalopathies is
slowing of the normal background frequency.
• Reactivity to photic or other type of external stimulation may be
altered.
• Some conditions are associated with an increase in seizure frequency,
and in such cases, epileptic activity may be recorded.
EEG findings
• Triphasic has been associated with a wide range of toxic, metabolic,
and structural abnormalities.
• Triphasic waves are associated with an altered level of consciousness
that may range from mild confusion to deep coma.
• The background may be slower in hepatic failure
• A classic etiology of triphasic wave is hepatic/metabolic
encephalopathy.
• Triphasic’s are high-amplitude (>70 µV).
• Having three phase +ive, -ive and then +ive.
• Initial sharp component.
Clinical and electrographical features
• There is good correlation b/w the severity of the EEG changes , the severity of the
encephalopathy and the clinical state of the patient. *
• Degree of impairment is clinically categorized as—
• *Coma
• *Stupourous.
• *Lethargy/ hyper-somnia
• *Confusion
• *Delirium *
• Degree of impairment is Electrographically categorized as,
• 1.Background slowing without theta delta slow waves.
• 2.Diffuse theta delta activity associated with normal background activity.
• 3.Slow background activity with diffuse theta delta activity.
Clinical and electrographical features &
possible pathologies
• Background slowing--- cortical (gray matter) dysfunction
• Delta theta slow waves – (Brain) white matter disease
• Delta theta slow waves , along with slow background activity--- both
cortical and white matter disease
• Serial EEGs needed to evaluate the course of disease process
Grading of EEG abnormalities in diffuse
encephalopathy
• 1 a --slow background 7-8 Hz without theta delta waves
• 1b —4-6 Hz background without theta delta waves
• 2a —dominant theta delta with normal background activity.
• 2b —dominant theta delta with slow background activity
• 3a--dominant delta with normal background activity
• 3b—dominant delta with slow background activity
• 4a —moderate to high amplitude delta >50 microvolt with no background reactivity
• 4b —low amplitude < 5sec
• 5a —burst suppression with suppression period < 5sec
• 5b —burst suppression with suppression period >5 sec.
• 6a —near electro cerebral silence.
• 6b --ECS
Burst suppression pattern
• Recurrent, periodic or pseudo periodic bursts with EEG suppression
period of variable duration
• Burst can be a mixture of sharp, spike, alpha. theta, delta activities
• The suppression period can last from 2s to 20 mint.
• Seen in Anoxic brain damage, CNS supressant drugs and severe
hypothermia
• Paradoxical arousal response
• A stimulus brings out slower activity with generalized high voltage
delta bursts, that is called as paradoxical arousal response
Triphasic waves
• Typical and atypical--- *
• Typical –initial small negative sharp discharges of 2-4 Hz, followed by large
positive sharp discharge and subsequent negative wave. *Frontal
dominant, Continuous, stereotyped ,forms a phase lag from anterior to
posterior region, seen in hepatic encephalopathy. *
• Atypical—less continuous, less stereotyped ,present in uremic,
hyperthyroid, toxic encephalopathies
• *In dementia (AD) posterior dominant triphasics are present.
• TW are also seen in encephalopathies associated with renal failure or
electrolyte imbalance, as well as anoxia and intoxications (such as lithium,
metrizamide, and levodopa)
ECS
• *No EEG activity over 2 micro volts when recorded from scalp
electrode pairs 10 cm interelectrodes distance.
• *Filter settings should not b below 30 Hz and low filter should not be
higher than 1 Hz.
• *Recording should be at-least one hour, with artifacts free 30 min
recording on 2uv.
• *Electrodes impedance should be 100ohm to 10Kohm.
References
• Practical Guide for Clinical Neurophysiologic Testing: EEG: Thoru
Yamada MD.
• *Basic Principles, Clinical Applications, and Related Fields
• *By Ernst Niedermeyer
• nelson text book of paediatrics 19th edition
Hashimoto’s Encephalopathy
• Steroid responsive acute or subacute encephalopathy associated with
anti-thyroid antibodies.
• Presenting features vary widely.
• Psychiatric symptoms around 60%.
• TPO and Thyroglobulin.
• TSH should be high but patients may be euthyroid or hypothyroid.
• Myxedema coma – acute or subacute and precipitated by stress.
• Hypothermic, Hypo ventilate, and “suspended animation.”
Hyper-Hypoglycemia
• Hyperosmolality
• Diabetic ketoacidosis – pH doesn’t correlate well with level of
consciousness.
• Diabetic lactic acidosis.
• Sudden lowering of serum osmolality – cerebral edema – can be fatal.
• Head trauma and Stroke patients – Glucose control.
Hypoglycemia
• Stroke like illness.
• Delirium.
• Coma.
• Seizure.
Hyperglycemia
• Seizures
• Hemianopia
• Hemichorea/Hemiballismus
Hypoglycemic Brain Injury
• Range from reversible focal deficits and transient encephalopathy to
irreversible coma.
• Mean blood glucose was around 30mg/dl.
• White matter – more sensitive to ischemia than previously thought.
• The duration of hypoglycemia may be difficult to determine in many
cases.
Hypoxic ischemic encephalopathy
• Abnormal neurological behaviour in the neonatal period arising as a
result of a hypoxic-ischemic event.
• Occurs in1-6 per 1000 term live births in developed countries
• 25% die or have multiple disabilities
• 4% have mild to moderate forms of cerebral palsy
• Essential criteria for diagnosis of HIE:
- metabolic acidosis
-early onset of encephalopathy
-Multisystem organ failure
Diagnosis
• Mri is the preferred imaging modality in neonates with HIE
• CT scan : identifies focal hemorrhagic lesions, diffuse cortical injury
and damage to the basal ganglia.
• aEEG : determine which infant are at high risk for long term brain
injury.
Treatment
1.hypothermia
2.Drug therapy : phenobarbital,phenytoin
3. Supportive care
WERNICKE ENCEPHALOPATHY
• WE is an acute, potentially reversible, neuropsychiatric disorder
caused by thiamine deficiency.
• The incidence can be as high as 12.5%
• The altered cognition of WE can progress to KS, a chronic and usually
permanent.
• Approximately 80% of patients with acute WE will develop KS.
• Mechanism:- Chronic alcoholism – Malnutrition – reduced thiamine
uptake and utilization
Physical examination
• The classical triad of symptoms – only 1/3rd of cases
• Ocular abnormalities – nystagmus, bilateral lateral rectus palsies,
conjugate gaze palsies, sluggish pupils, ptosis, and anisocoria
• Encephalopathy – global confusionalstate, disinterest,
inattentiveness, or agitation; Coma is rare.
• Gait ataxia – cerebellar damage, and vestibular paresis
• Peripheral neuropathy – foot drop, and decreased proprioception
Management
• Erythrocyte transketolase activity assay, Thiamine assay – very specific tests – not widely
available – reserved for diagnostic dilemmas
• EEG and CSF analysis may exclude other explanatory or concomitant conditions.
• Emergency department care – Parenteral thiamine –Requirement in chronic alcoholics
may be as high as 500mg single dose or multiple daily doses.
• Never start on Dextrose
• Treatment with thiamine repletion, currently recommended at 1 gram of IV thiamine per
24 hours for alcoholics with suspected Wernicke encephalopathy , should not be delayed.
• Death occurs in nearly 20 % of patients with delayed treatment.
• In-Patient care –Watch for complications – Korsakoff psychosis –Alcohol withdrawal –
Congestive heart failure – Lactic acidosis
• Out-Patient Care – Thiamine 100 mg PO daily, start alcohol cessation program, Advise on
importance of balanced diet.
Refrences
• Practical Guide for Clinical Neurophysiologic Testing: EEG: Thoru
Yamada MD.
• Basic Principles, Clinical Applications, and Related Fields
• By Ernst Niedermeyer
• nelson text book of paediatrics 19th edition
Thank you

Weitere ähnliche Inhalte

Was ist angesagt?

Was ist angesagt? (20)

Traumatic head injury
Traumatic head injuryTraumatic head injury
Traumatic head injury
 
Seizures
SeizuresSeizures
Seizures
 
Brain abscess
Brain abscessBrain abscess
Brain abscess
 
Intracerebral hemorhage Diagnosis and management
Intracerebral hemorhage  Diagnosis and managementIntracerebral hemorhage  Diagnosis and management
Intracerebral hemorhage Diagnosis and management
 
Subdural hematoma
Subdural hematomaSubdural hematoma
Subdural hematoma
 
Cva
CvaCva
Cva
 
Hemorrhagic stroke
Hemorrhagic   strokeHemorrhagic   stroke
Hemorrhagic stroke
 
Head injury
Head injuryHead injury
Head injury
 
TIA
TIATIA
TIA
 
Traumatic brain injury
Traumatic brain injuryTraumatic brain injury
Traumatic brain injury
 
Ischaemic stroke
Ischaemic stroke Ischaemic stroke
Ischaemic stroke
 
Myasthenia gravis
Myasthenia gravisMyasthenia gravis
Myasthenia gravis
 
BRAIN ABSCESS
BRAIN ABSCESSBRAIN ABSCESS
BRAIN ABSCESS
 
Approach to seizure
Approach to seizureApproach to seizure
Approach to seizure
 
Dementia PRESENTATION
Dementia PRESENTATIONDementia PRESENTATION
Dementia PRESENTATION
 
Status epilepticus
Status epilepticusStatus epilepticus
Status epilepticus
 
Spinal cord injury
Spinal cord injurySpinal cord injury
Spinal cord injury
 
Spinal cord injury (SCI)
Spinal cord injury (SCI)Spinal cord injury (SCI)
Spinal cord injury (SCI)
 
Neuroleptic Malignant Syndrome
Neuroleptic Malignant Syndrome Neuroleptic Malignant Syndrome
Neuroleptic Malignant Syndrome
 
Increased Intracranial Pressure
Increased Intracranial PressureIncreased Intracranial Pressure
Increased Intracranial Pressure
 

Ähnlich wie ENCEPHALOPATHY

HEPATIC ENCEPHALOPATHY
HEPATIC ENCEPHALOPATHYHEPATIC ENCEPHALOPATHY
HEPATIC ENCEPHALOPATHYOluwatomisin1
 
Approach to an unconcious child
Approach to an unconcious childApproach to an unconcious child
Approach to an unconcious childNishant Yadav
 
Metabolic encephalopathies 2
Metabolic encephalopathies 2Metabolic encephalopathies 2
Metabolic encephalopathies 2Riham Nasar
 
Central Nervous System, Epilepsy, Parkinson, Alzheimer, Stroke and Migraine.
Central Nervous System, Epilepsy, Parkinson, Alzheimer, Stroke and Migraine.Central Nervous System, Epilepsy, Parkinson, Alzheimer, Stroke and Migraine.
Central Nervous System, Epilepsy, Parkinson, Alzheimer, Stroke and Migraine.Dr. Kiran Dhamak
 
Antiepileptic drugs.pptx
Antiepileptic drugs.pptxAntiepileptic drugs.pptx
Antiepileptic drugs.pptxSejalkhumam
 
Epilepsy – A Modern Day Perspective
Epilepsy – A Modern Day PerspectiveEpilepsy – A Modern Day Perspective
Epilepsy – A Modern Day PerspectiveVivek Misra
 
Epilepsy
EpilepsyEpilepsy
EpilepsyM S
 
AlharebEpilepsy(1).pptx
AlharebEpilepsy(1).pptxAlharebEpilepsy(1).pptx
AlharebEpilepsy(1).pptxAhmedalmahdi16
 
Lecture 12. Antiepileptic drugs pharmacology.pptx
Lecture 12. Antiepileptic drugs pharmacology.pptxLecture 12. Antiepileptic drugs pharmacology.pptx
Lecture 12. Antiepileptic drugs pharmacology.pptxsathishvsathish1
 
Kegawatdaruratan Neurologi copy.ppt
Kegawatdaruratan Neurologi copy.pptKegawatdaruratan Neurologi copy.ppt
Kegawatdaruratan Neurologi copy.pptKevinTandarto1
 
Kegawatdaruratan Neurologi copy.ppt
Kegawatdaruratan Neurologi copy.pptKegawatdaruratan Neurologi copy.ppt
Kegawatdaruratan Neurologi copy.pptHarrisMurdianto2
 
Kegawatdaruratan Neurologi copy(1).ppt
Kegawatdaruratan Neurologi copy(1).pptKegawatdaruratan Neurologi copy(1).ppt
Kegawatdaruratan Neurologi copy(1).pptArinta3
 

Ähnlich wie ENCEPHALOPATHY (20)

ENCEPHALOPATHY
ENCEPHALOPATHY ENCEPHALOPATHY
ENCEPHALOPATHY
 
HEPATIC ENCEPHALOPATHY
HEPATIC ENCEPHALOPATHYHEPATIC ENCEPHALOPATHY
HEPATIC ENCEPHALOPATHY
 
Seizure disorders
Seizure disordersSeizure disorders
Seizure disorders
 
Approach to an unconcious child
Approach to an unconcious childApproach to an unconcious child
Approach to an unconcious child
 
Seizure.pptx
Seizure.pptxSeizure.pptx
Seizure.pptx
 
Metabolic encephalopathies 2
Metabolic encephalopathies 2Metabolic encephalopathies 2
Metabolic encephalopathies 2
 
EPILEPSY
EPILEPSYEPILEPSY
EPILEPSY
 
Central Nervous System, Epilepsy, Parkinson, Alzheimer, Stroke and Migraine.
Central Nervous System, Epilepsy, Parkinson, Alzheimer, Stroke and Migraine.Central Nervous System, Epilepsy, Parkinson, Alzheimer, Stroke and Migraine.
Central Nervous System, Epilepsy, Parkinson, Alzheimer, Stroke and Migraine.
 
Antiepileptic drugs.pptx
Antiepileptic drugs.pptxAntiepileptic drugs.pptx
Antiepileptic drugs.pptx
 
Epilepsy – A Modern Day Perspective
Epilepsy – A Modern Day PerspectiveEpilepsy – A Modern Day Perspective
Epilepsy – A Modern Day Perspective
 
Dr. Surendra SGPGI
Dr. Surendra SGPGIDr. Surendra SGPGI
Dr. Surendra SGPGI
 
AE FINAL.pptx
AE FINAL.pptxAE FINAL.pptx
AE FINAL.pptx
 
Epilepsy
EpilepsyEpilepsy
Epilepsy
 
AlharebEpilepsy(1).pptx
AlharebEpilepsy(1).pptxAlharebEpilepsy(1).pptx
AlharebEpilepsy(1).pptx
 
Coma final
Coma  finalComa  final
Coma final
 
Seizures
SeizuresSeizures
Seizures
 
Lecture 12. Antiepileptic drugs pharmacology.pptx
Lecture 12. Antiepileptic drugs pharmacology.pptxLecture 12. Antiepileptic drugs pharmacology.pptx
Lecture 12. Antiepileptic drugs pharmacology.pptx
 
Kegawatdaruratan Neurologi copy.ppt
Kegawatdaruratan Neurologi copy.pptKegawatdaruratan Neurologi copy.ppt
Kegawatdaruratan Neurologi copy.ppt
 
Kegawatdaruratan Neurologi copy.ppt
Kegawatdaruratan Neurologi copy.pptKegawatdaruratan Neurologi copy.ppt
Kegawatdaruratan Neurologi copy.ppt
 
Kegawatdaruratan Neurologi copy(1).ppt
Kegawatdaruratan Neurologi copy(1).pptKegawatdaruratan Neurologi copy(1).ppt
Kegawatdaruratan Neurologi copy(1).ppt
 

Mehr von NeurologyKota

CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptx
CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptxCONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptx
CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptxNeurologyKota
 
NEUROLOGICAL SCALES FOR ASSESSMENT OF CONSCIOUSNESS.pptx
NEUROLOGICAL SCALES FOR ASSESSMENT OF CONSCIOUSNESS.pptxNEUROLOGICAL SCALES FOR ASSESSMENT OF CONSCIOUSNESS.pptx
NEUROLOGICAL SCALES FOR ASSESSMENT OF CONSCIOUSNESS.pptxNeurologyKota
 
LOCALISATION OF LESION CAUSING COMA.pptx
LOCALISATION OF LESION CAUSING COMA.pptxLOCALISATION OF LESION CAUSING COMA.pptx
LOCALISATION OF LESION CAUSING COMA.pptxNeurologyKota
 
TREADMILL For_BRAIN_Dr Bharat Bhushan sir.pptx
TREADMILL For_BRAIN_Dr Bharat Bhushan sir.pptxTREADMILL For_BRAIN_Dr Bharat Bhushan sir.pptx
TREADMILL For_BRAIN_Dr Bharat Bhushan sir.pptxNeurologyKota
 
DUAL AND TRIPLE ANTITHROMBOTIC THERAPY FOR SECONDARY STROKE [Autosaved].pptx
DUAL AND TRIPLE ANTITHROMBOTIC THERAPY FOR SECONDARY STROKE [Autosaved].pptxDUAL AND TRIPLE ANTITHROMBOTIC THERAPY FOR SECONDARY STROKE [Autosaved].pptx
DUAL AND TRIPLE ANTITHROMBOTIC THERAPY FOR SECONDARY STROKE [Autosaved].pptxNeurologyKota
 
SMART WEARABLE DEVICES IN NEUROLOGY new.pptx
SMART WEARABLE DEVICES IN NEUROLOGY new.pptxSMART WEARABLE DEVICES IN NEUROLOGY new.pptx
SMART WEARABLE DEVICES IN NEUROLOGY new.pptxNeurologyKota
 
ASSESSMENT OF AUTONOMIC FUNCTION TEST.pptx
ASSESSMENT OF AUTONOMIC FUNCTION TEST.pptxASSESSMENT OF AUTONOMIC FUNCTION TEST.pptx
ASSESSMENT OF AUTONOMIC FUNCTION TEST.pptxNeurologyKota
 
TRANSCRANIAL DOPPLER (1).pptx
TRANSCRANIAL DOPPLER (1).pptxTRANSCRANIAL DOPPLER (1).pptx
TRANSCRANIAL DOPPLER (1).pptxNeurologyKota
 
INTRACEREBRAL HEMORRHAGE IN YOUNG ADULTS.pptx
INTRACEREBRAL HEMORRHAGE IN YOUNG ADULTS.pptxINTRACEREBRAL HEMORRHAGE IN YOUNG ADULTS.pptx
INTRACEREBRAL HEMORRHAGE IN YOUNG ADULTS.pptxNeurologyKota
 
EPILEPTIC ENCEPHALOPATHY
 EPILEPTIC ENCEPHALOPATHY  EPILEPTIC ENCEPHALOPATHY
EPILEPTIC ENCEPHALOPATHY NeurologyKota
 
Domain Assessment in Dementia.pptx
Domain Assessment in Dementia.pptxDomain Assessment in Dementia.pptx
Domain Assessment in Dementia.pptxNeurologyKota
 
Young Onset Dementia.pptx
Young Onset Dementia.pptxYoung Onset Dementia.pptx
Young Onset Dementia.pptxNeurologyKota
 
NEWER INSIGHT IN FUNCTIONAL NEUROLOGICAL DISORDER
NEWER INSIGHT IN FUNCTIONAL NEUROLOGICAL DISORDER NEWER INSIGHT IN FUNCTIONAL NEUROLOGICAL DISORDER
NEWER INSIGHT IN FUNCTIONAL NEUROLOGICAL DISORDER NeurologyKota
 
Hyperthermic syndrome in ICU and their management.pptx
Hyperthermic syndrome in ICU and their management.pptxHyperthermic syndrome in ICU and their management.pptx
Hyperthermic syndrome in ICU and their management.pptxNeurologyKota
 
Entrapment Syndromes of Lower Limb.pptx
Entrapment Syndromes of Lower Limb.pptxEntrapment Syndromes of Lower Limb.pptx
Entrapment Syndromes of Lower Limb.pptxNeurologyKota
 
MOG and IgG-4 related Neurological manifestation.pptx
MOG and IgG-4 related Neurological manifestation.pptxMOG and IgG-4 related Neurological manifestation.pptx
MOG and IgG-4 related Neurological manifestation.pptxNeurologyKota
 

Mehr von NeurologyKota (20)

CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptx
CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptxCONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptx
CONCEPT OF NODOPATHIES AND PARANODOPATHIES.pptx
 
NEUROLOGICAL SCALES FOR ASSESSMENT OF CONSCIOUSNESS.pptx
NEUROLOGICAL SCALES FOR ASSESSMENT OF CONSCIOUSNESS.pptxNEUROLOGICAL SCALES FOR ASSESSMENT OF CONSCIOUSNESS.pptx
NEUROLOGICAL SCALES FOR ASSESSMENT OF CONSCIOUSNESS.pptx
 
LOCALISATION OF LESION CAUSING COMA.pptx
LOCALISATION OF LESION CAUSING COMA.pptxLOCALISATION OF LESION CAUSING COMA.pptx
LOCALISATION OF LESION CAUSING COMA.pptx
 
TREADMILL For_BRAIN_Dr Bharat Bhushan sir.pptx
TREADMILL For_BRAIN_Dr Bharat Bhushan sir.pptxTREADMILL For_BRAIN_Dr Bharat Bhushan sir.pptx
TREADMILL For_BRAIN_Dr Bharat Bhushan sir.pptx
 
REMOTE ROBOTIC.pptx
REMOTE ROBOTIC.pptxREMOTE ROBOTIC.pptx
REMOTE ROBOTIC.pptx
 
DUAL AND TRIPLE ANTITHROMBOTIC THERAPY FOR SECONDARY STROKE [Autosaved].pptx
DUAL AND TRIPLE ANTITHROMBOTIC THERAPY FOR SECONDARY STROKE [Autosaved].pptxDUAL AND TRIPLE ANTITHROMBOTIC THERAPY FOR SECONDARY STROKE [Autosaved].pptx
DUAL AND TRIPLE ANTITHROMBOTIC THERAPY FOR SECONDARY STROKE [Autosaved].pptx
 
SMART WEARABLE DEVICES IN NEUROLOGY new.pptx
SMART WEARABLE DEVICES IN NEUROLOGY new.pptxSMART WEARABLE DEVICES IN NEUROLOGY new.pptx
SMART WEARABLE DEVICES IN NEUROLOGY new.pptx
 
ASSESSMENT OF AUTONOMIC FUNCTION TEST.pptx
ASSESSMENT OF AUTONOMIC FUNCTION TEST.pptxASSESSMENT OF AUTONOMIC FUNCTION TEST.pptx
ASSESSMENT OF AUTONOMIC FUNCTION TEST.pptx
 
TRANSCRANIAL DOPPLER (1).pptx
TRANSCRANIAL DOPPLER (1).pptxTRANSCRANIAL DOPPLER (1).pptx
TRANSCRANIAL DOPPLER (1).pptx
 
INTRACEREBRAL HEMORRHAGE IN YOUNG ADULTS.pptx
INTRACEREBRAL HEMORRHAGE IN YOUNG ADULTS.pptxINTRACEREBRAL HEMORRHAGE IN YOUNG ADULTS.pptx
INTRACEREBRAL HEMORRHAGE IN YOUNG ADULTS.pptx
 
CAROTID WEB.pptx
CAROTID WEB.pptxCAROTID WEB.pptx
CAROTID WEB.pptx
 
CNS IRIS.pptx
CNS IRIS.pptxCNS IRIS.pptx
CNS IRIS.pptx
 
EPILEPTIC ENCEPHALOPATHY
 EPILEPTIC ENCEPHALOPATHY  EPILEPTIC ENCEPHALOPATHY
EPILEPTIC ENCEPHALOPATHY
 
Domain Assessment in Dementia.pptx
Domain Assessment in Dementia.pptxDomain Assessment in Dementia.pptx
Domain Assessment in Dementia.pptx
 
Young Onset Dementia.pptx
Young Onset Dementia.pptxYoung Onset Dementia.pptx
Young Onset Dementia.pptx
 
NEWER INSIGHT IN FUNCTIONAL NEUROLOGICAL DISORDER
NEWER INSIGHT IN FUNCTIONAL NEUROLOGICAL DISORDER NEWER INSIGHT IN FUNCTIONAL NEUROLOGICAL DISORDER
NEWER INSIGHT IN FUNCTIONAL NEUROLOGICAL DISORDER
 
Hyperthermic syndrome in ICU and their management.pptx
Hyperthermic syndrome in ICU and their management.pptxHyperthermic syndrome in ICU and their management.pptx
Hyperthermic syndrome in ICU and their management.pptx
 
Entrapment Syndromes of Lower Limb.pptx
Entrapment Syndromes of Lower Limb.pptxEntrapment Syndromes of Lower Limb.pptx
Entrapment Syndromes of Lower Limb.pptx
 
MOG and IgG-4 related Neurological manifestation.pptx
MOG and IgG-4 related Neurological manifestation.pptxMOG and IgG-4 related Neurological manifestation.pptx
MOG and IgG-4 related Neurological manifestation.pptx
 
BRAIN DEATH.pptx
BRAIN DEATH.pptxBRAIN DEATH.pptx
BRAIN DEATH.pptx
 

Kürzlich hochgeladen

raisen Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
raisen Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetraisen Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
raisen Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
neemuch Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
neemuch Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetneemuch Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
neemuch Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
bhopal Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
bhopal Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetbhopal Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
bhopal Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
Premium Call Girls Bangalore {7304373326} ❤️VVIP POOJA Call Girls in Bangalor...
Premium Call Girls Bangalore {7304373326} ❤️VVIP POOJA Call Girls in Bangalor...Premium Call Girls Bangalore {7304373326} ❤️VVIP POOJA Call Girls in Bangalor...
Premium Call Girls Bangalore {7304373326} ❤️VVIP POOJA Call Girls in Bangalor...Sheetaleventcompany
 
jabalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
jabalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetjabalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
jabalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
(Deeksha) 💓 9920725232 💓High Profile Call Girls Navi Mumbai You Can Get The S...
(Deeksha) 💓 9920725232 💓High Profile Call Girls Navi Mumbai You Can Get The S...(Deeksha) 💓 9920725232 💓High Profile Call Girls Navi Mumbai You Can Get The S...
(Deeksha) 💓 9920725232 💓High Profile Call Girls Navi Mumbai You Can Get The S...Ahmedabad Call Girls
 
Thoothukudi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Thoothukudi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetThoothukudi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Thoothukudi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
Mangalore Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Mangalore Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetMangalore Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Mangalore Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
Kochi call girls Mallu escort girls available 7877702510
Kochi call girls Mallu escort girls available 7877702510Kochi call girls Mallu escort girls available 7877702510
Kochi call girls Mallu escort girls available 7877702510Vipesco
 
💚 Punjabi Call Girls In Chandigarh 💯Lucky 🔝8868886958🔝Call Girl In Chandigarh
💚 Punjabi Call Girls In Chandigarh 💯Lucky 🔝8868886958🔝Call Girl In Chandigarh💚 Punjabi Call Girls In Chandigarh 💯Lucky 🔝8868886958🔝Call Girl In Chandigarh
💚 Punjabi Call Girls In Chandigarh 💯Lucky 🔝8868886958🔝Call Girl In ChandigarhSheetaleventcompany
 
Mathura Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Mathura Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetMathura Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Mathura Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
Patna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Patna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetPatna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Patna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
Jalna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Jalna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetJalna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Jalna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
dhanbad Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
dhanbad Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetdhanbad Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
dhanbad Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
Call Girl in Bangalore 9632137771 {LowPrice} ❤️ (Navya) Bangalore Call Girls ...
Call Girl in Bangalore 9632137771 {LowPrice} ❤️ (Navya) Bangalore Call Girls ...Call Girl in Bangalore 9632137771 {LowPrice} ❤️ (Navya) Bangalore Call Girls ...
Call Girl in Bangalore 9632137771 {LowPrice} ❤️ (Navya) Bangalore Call Girls ...mahaiklolahd
 
kochi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
kochi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetkochi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
kochi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
Russian Call Girls in Noida Pallavi 9711199171 High Class Call Girl Near Me
Russian Call Girls in Noida Pallavi 9711199171 High Class Call Girl Near MeRussian Call Girls in Noida Pallavi 9711199171 High Class Call Girl Near Me
Russian Call Girls in Noida Pallavi 9711199171 High Class Call Girl Near Memriyagarg453
 
Krishnagiri call girls Tamil Actress sex service 7877702510
Krishnagiri call girls Tamil Actress sex service 7877702510Krishnagiri call girls Tamil Actress sex service 7877702510
Krishnagiri call girls Tamil Actress sex service 7877702510Vipesco
 
Bihar Sharif Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Bihar Sharif Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetBihar Sharif Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Bihar Sharif Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 
Sambalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Sambalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetSambalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Sambalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetCall Girls Service
 

Kürzlich hochgeladen (20)

raisen Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
raisen Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetraisen Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
raisen Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
neemuch Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
neemuch Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetneemuch Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
neemuch Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
bhopal Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
bhopal Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetbhopal Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
bhopal Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
Premium Call Girls Bangalore {7304373326} ❤️VVIP POOJA Call Girls in Bangalor...
Premium Call Girls Bangalore {7304373326} ❤️VVIP POOJA Call Girls in Bangalor...Premium Call Girls Bangalore {7304373326} ❤️VVIP POOJA Call Girls in Bangalor...
Premium Call Girls Bangalore {7304373326} ❤️VVIP POOJA Call Girls in Bangalor...
 
jabalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
jabalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetjabalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
jabalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
(Deeksha) 💓 9920725232 💓High Profile Call Girls Navi Mumbai You Can Get The S...
(Deeksha) 💓 9920725232 💓High Profile Call Girls Navi Mumbai You Can Get The S...(Deeksha) 💓 9920725232 💓High Profile Call Girls Navi Mumbai You Can Get The S...
(Deeksha) 💓 9920725232 💓High Profile Call Girls Navi Mumbai You Can Get The S...
 
Thoothukudi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Thoothukudi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetThoothukudi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Thoothukudi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
Mangalore Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Mangalore Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetMangalore Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Mangalore Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
Kochi call girls Mallu escort girls available 7877702510
Kochi call girls Mallu escort girls available 7877702510Kochi call girls Mallu escort girls available 7877702510
Kochi call girls Mallu escort girls available 7877702510
 
💚 Punjabi Call Girls In Chandigarh 💯Lucky 🔝8868886958🔝Call Girl In Chandigarh
💚 Punjabi Call Girls In Chandigarh 💯Lucky 🔝8868886958🔝Call Girl In Chandigarh💚 Punjabi Call Girls In Chandigarh 💯Lucky 🔝8868886958🔝Call Girl In Chandigarh
💚 Punjabi Call Girls In Chandigarh 💯Lucky 🔝8868886958🔝Call Girl In Chandigarh
 
Mathura Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Mathura Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetMathura Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Mathura Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
Patna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Patna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetPatna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Patna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
Jalna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Jalna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetJalna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Jalna Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
dhanbad Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
dhanbad Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetdhanbad Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
dhanbad Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
Call Girl in Bangalore 9632137771 {LowPrice} ❤️ (Navya) Bangalore Call Girls ...
Call Girl in Bangalore 9632137771 {LowPrice} ❤️ (Navya) Bangalore Call Girls ...Call Girl in Bangalore 9632137771 {LowPrice} ❤️ (Navya) Bangalore Call Girls ...
Call Girl in Bangalore 9632137771 {LowPrice} ❤️ (Navya) Bangalore Call Girls ...
 
kochi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
kochi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meetkochi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
kochi Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
Russian Call Girls in Noida Pallavi 9711199171 High Class Call Girl Near Me
Russian Call Girls in Noida Pallavi 9711199171 High Class Call Girl Near MeRussian Call Girls in Noida Pallavi 9711199171 High Class Call Girl Near Me
Russian Call Girls in Noida Pallavi 9711199171 High Class Call Girl Near Me
 
Krishnagiri call girls Tamil Actress sex service 7877702510
Krishnagiri call girls Tamil Actress sex service 7877702510Krishnagiri call girls Tamil Actress sex service 7877702510
Krishnagiri call girls Tamil Actress sex service 7877702510
 
Bihar Sharif Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Bihar Sharif Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetBihar Sharif Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Bihar Sharif Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 
Sambalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Sambalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real MeetSambalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
Sambalpur Call Girls 👙 6297143586 👙 Genuine WhatsApp Number for Real Meet
 

ENCEPHALOPATHY

  • 1. ENCEPHALOPATHY: TYPES, SYMPTOMS, CAUSES, STAGES & TREATMENT  Derived from Greek word “enkephalos”- meaning brain.  “Pathos” meaning is disease.  The term “encephalopathy” is defined as altered mental status as a result of a diffuse disturbance of brain function.  It represents a brain state in which normal functioning of the brain is disturbed temporarily or permanently.  Any clinical condition that causes impairment in consciousness usually accompanied by diffuse EEG abnormalities
  • 2. Types & Causes of encephalopathy  Reversible  metabolic encephalopathy,  Hashimoto’s encephalopathy,  hepatic encephalopathy,  infectious of the brain,  brain tumours,  toxic encephalopathy,  nonconvulsive status epilepticus  Irreversible chronic traumatic encephalopathy Hypoxic-ischemic encephalopathy
  • 3. Causes of encephalopathy • Encephalopathy results main from, • Metabolic derangements (Na, K, Ca) • Toxins (exposure to toxic substances, e.g lithium paints, industrial • chemicals) • infectious (bacteria (TB) viruses, parasites, or prions), • Hepatic (liver failure or liver cancer) • Inflammations (Systemic Lupus Erythropetosis, sarcoidosis (soft • tissues diseases) • Drug Induced (Over dozage of the drug) • Demyelinating (e.g MS) • Degenerative processes (Alzheimer disease, Parkinson's disease) • Anoxic encephalopathy (lack of oxygen to the brain, including traumatic • causes) • Hereditary encephalopathies (leucodystrophy white matter)
  • 4. SYMPTOMS  Common symptoms • confusion • memory loss • personality changes • troubling in thinking or focusing  Less common symptoms • trouble in speaking • muscle weakness or twitches • tremors • seizures • sleepiness
  • 5. Hepatic encephalopathy Definition: Hepatic encephalopathy is a reversible neuropsychiatric state that complicates severe liver disease. • Encephalopathy associated with Cirrhosis and portal hypertension • Encephalopathy associated with portal systemic Bypass without hepatocellular disease • Encephalopathy associated with Acute liver failure
  • 6. Clinical features 1. Disturbed consciousness: Sleep disturbance (change of sleep pattern to hypersomnia , or drowsiness ) Confusion including delirium Unconscious 2. Abnormal behavior 3. Intellectual deterioration (cognition) 4. Abnormal nerve reflexes Flapping tremor (asterixis)
  • 7. Clinical grading • Stage 1: Abnormal sleep, Abnormal behavior (mood change e.g. euphoria/depression, strange behavior ) Altered cognition ( decreased attention and calculation ability) Flapping tremor (+/-) EEG (+/-) • Stage 2: Lethargic, Inappropriate behavior Disorientation and memory decreased Flapping tremor (+), abnormal nerve reflexes(ataxia) EEG (+) Clinical grading • Stage 3: Somnolence but can be aroused, marked confusion (delirium) Flapping tremor (+), abnormal nerve reflexes EEG (+) • Stage 4: unconsciousness (can not be aroused) abnormal to loss of reflexes
  • 8. Investigation • 1. Blood ammonia • 2.Electroencephalogram • 3. Evoked potentials • 4. Psychometric tests
  • 9. Treatment . Identification & correction of the precipitating cause: • Precipitating factors • Drugs! • Electrolyte imbalance – hypokalemia/metabolic alkalosis (diuretics, vomiting, diarrhea, infusion) • GI Bleeding Infection • Constipation • Large protein meal
  • 10. Cont.  Intervention to reduce the production & absorption of gut-derived ammonia & other toxins: • 1) Diet: reduce and modify dietary protein and maintain Calorie intake • 2) Enemas (mild acid) and/or purgation • 3) Lactulose or lactitol • 4) Inhibition of gut bacteria: Antibiotics: neomycin(oral), metronidazone? • 5) Modification of colonic flora: probiotics? Modify colonic flora, resulting in displacement of urease-containing bacteria with lactobacillus Cathartic effect Lower the colonic pH, resulting in the formation of non-absorbable NH4 from NH3 in the colon
  • 11. Metabolic encephalopathy Pathophysiology: • Mainly it depends on the cause However regardless the etiology the main mechanism is due to disruption of arousal and attention centers in the brain (ARAS). • Another mechanism including compression or injury for areas critical for memory ,attention and executive functions . • Abnormalities in neurotransmitters such as ( (Ach , serotonin, GABA ,dopamine, tryptophan ,cytokines ) also affect these connections.
  • 12. Uremic encephalopathy Pathology : • Decrease clearance of osmotically active toxins • Proinflammatory state lead to BBB breakage • Electrolytes abnormailites • Seziures and myoclonus • Dysequilibrium syndrome • Dialysis dementia • Cerebral atrophy
  • 13. symptoms: • Seizures and myoclonus • Permanent memory loss • Dysarthria • Facial grimacing • Myoclonus • Mood and personality changes • Confusion • Headache • Nausea and vomiting • Tremors
  • 14. Prognosis: • Metabolic encephalopathy is common in the ICU setting • the brain dysfunction that occurs with metabolic encephalopathy was thought to be completely reversible • critically ill patients with metabolic encephalopathy are often left with long-term neurocognitive deficits. • Persistent neurologic and psychiatric deficits occur in up to 32% of medical ICU survivors
  • 15. Management: • Any of abnormal movement presented in renal patient should be evaluated by EEG confirm diagnosis of myoclonus • • Phenytoin used as AEDs in uremic patient to control sezuires but it worse myoclonus • • Best choice for myoclonus is tiratam &valporic acid
  • 16. HASHIMOTO ENCEPHALOPATHY • Defined by the detection of thyroid peroxidase (TPO) antibodies in patients with acute or subacute encephalitis that responds to steroids. • “Encephalopathy associated with autoimmune thyroid disease” is considered more accurate- due to normal thyroid function. • Very vague symptoms- unclear course
  • 17. Clinical features: non specific • Stroke-like symptoms • Tremor, myoclonus • Transient aphasia • Sleep and behaviour abnormalities • Hallucinations, seizures and ataxia.
  • 18. Diagnosis: • clinical triad of neuropsychiatric symptoms, detection of antimicrosomal or antithyroglobulin antibodies, and exclusion of other causes. • antithyroid peroxidase, antithyroglobulin, • lesser extent thyroid-stimulating hormone receptor • blocking antibodies. • α-enolase • CSF show moderately elevated protein, may be positive for anti thyroid Ab, OCB seen • EEG: slowing, triphasic waves, epileptiform discharges. • MRI usually normal, occasionally non-specific sub cortical white matter T2 signal changes. • Thyroid status may be normal.
  • 19. Treatment: • Initial treatment is usually with oral prednisone (50– 150 mg/day) or high-dose IV methylprednisolone (1 g/day) for 3–7 days. Thyroid hormone treatment is also included if required. • Failure of some patients to respond to this first line treatment has produced a variety of alternative treatments including azathioprine, cyclophosphamide, chloroquine, methotrexate, periodic intravenous immunoglobulin and plasma exchange. • Seizures, if present, are controlled with typical antiepileptic agents. • Recurrence – continued steroids, IVIG, other immunomodulatory drugs.
  • 20. NMDA ENCEPHALOPATHY • Leading cause of autoimmune encephalitis in children and adolescents. • Age- frequently 2– 40 years, 80% Female • Stages : • Stage1 – prodromal phase • Stage 2 – psychiatric and behavioral problems • Stage 3 – Decreased level of consciousness • Behavioral changes included new-onset temper tantrums, agitation, aggression, and changes in mood or personality
  • 21. Clinical features: • Behavioural disturbance,Psychosis • Catatonia • Seizures • Movement disorders including orolingual dyskinesias and stereotypic movement. • Dysautonomia. • Ovarian teratoma is associated in up to 50% of the cases
  • 22. Diagnosis • CSF : -lymphocytic pleocytosis, -elevated protein levels -oligoclonal bands • EEG – extreme delta brush • MRI demonstrate medial temporal lobe attenuated inversion recovery high signal or focal areas of hyperintensity in the frontal or parietal cortex • fluorodeoxyglucose positron emission tomography (FDG-PET) scan show cortical hypermetabolism in acute stages, and hypometabolism in more subacute stages of the illness.
  • 23. Treatment • first line of immunotherapies including corticosteroids, intravenous immunoglobulin, or plasma exchange • Rituximab and cyclophosphamide, alone or combined, are often effective in adults • Approximately 80% of patients have substantial or full recovery.
  • 24. Septic encephalopathy • The term "septic encephalopathy" : • acute confusional episodes or other significant cognitive abnormalities that develop during sepsis • as an entity that cannot be explained by hepatic or renal dysfunction, hypotension, or hypoxia • Occur in a range of 8–70% of septic patients • May as an early sign of sepsis • Imply poor prognosis , higher mortality
  • 25. Etiology and pathopysiology • Most likely multifactorial • Underlying mechanisms only been defined in parts • Disseminated cerebral microabscesses -infecting organisms and/or their toxins do not directly cause encephalopathy. • Systemic inflammation resulting from infection or other causes action of inflammatory mediators on the brain , cytotoxic response of brain cells
  • 26. Cont. • Free radicals • damage RBC and limit O2 delivery to brain • Inflammatory mediators • impair mitochondrial function and O2 extraction by the brain destroy BBB • perimicrovessel edema • disruption of astrocyte endfeet • aromatic a.a enter brain parenchyma and disturb NT • Ultimately, extensive neuronal injury
  • 27. Diagnosis No specific test available Electroencephalopathy • Most sensitive diagnostic tool • Normal, diffuse slowing,excessive theta,predominantly delta,triphasic waves, and suppression or burst suppression. • Evaluating depressed consciousness in critically ill p`ts • (1) Receiving sedative and narcotic drugs • (2) Head injury , intracranial event e.g. cerebrovascular causes • (3) Metabolic derangements : • Sugar , electrolytes (Na ,Ca) , acid-base balance (acidemia , hypercapnia), oxygenation (hypoxia ,hypotention) , hepatic encephalopathy ,uremic encephalopathy , septic encephalopathy , alcohol or drug • TREATMENT: According to cause of septicemia If hypotension start inotropic supports
  • 28. Question. • A 21-year-old primigravida with gestation age of 33weeks whose first and second trimester gestation was uneventful with no history of hypertension and epilepsy before and during pregnancy. She developed sudden onset of headache, giddiness, vomiting, and convulsions. Her blood pressure was 142/94 mmHg. Next day, the patient was taken into C section for fetal distress. On 2nd day of postcaesarean section she developed loss of vision, headache, and vomiting. Her blood pressure was 140/114 mmHg.
  • 29. PRES • Posterior Reversible Encephalopathy Syndrome. • Variety of symptoms – headache, altered mental status, visual disturbances, and seizures. • Hypertension, Pre-eclampsia/eclampsia, immunosuppression, sepsis, chemotherapy, collagen vascular disease, and renal failure.
  • 30. Question. • A 36-year-old real estate agent was in the first trimester of her first pregnancy when she awoke with diplopia. She had not been well for several days, feeling lethargic, off-balance and slightly disoriented; symptoms that she attributed to severe morning sickness during the previous eight weeks. She was not taking any medications and had been previously healthy. Exam revealed bilateral ptosis, limitation of gaze in all directions, slow upward saccades, upbeat nystagmus and mild ataxia.
  • 31. • Wernicke’s encephalopathy – • triad of ophthalmoplegia, ataxia, and confusion. O • Triad – minority of cases. O • Ocular findings – earliest and most constant. O • About 30% have isolated or predominant mental status changes ranging from confusion to frank coma. O • Sometimes – sudden onset.
  • 32. Mangement • Low serum erythrocyte transketolase – days to obtain. • Treat on suspicion. • MRI – specific (93%) but sensitivity is low.
  • 34. Clinical features: • Fever , headache • Meningism • Focal neurological deficits • Seizures • Primary source of infection • Pneumonia (bacteria, mycoplasma, TB), purpuric rash (meningococcemia), mucosal herpetic lesions, cyanotic heart dis. (brain abscess)
  • 35. Investigations: • CBC, CRP, ESR • Blood culture • Viral study (blood, throat, urine, stool) • TB work-up • CSF: ME, sugar, protein, C&S, virology, TB, fungus
  • 36. Tumour /CNS Malignancy • Suggestive features • Signs & symptoms of raised ICP • Focal neurological deficit • Seizures • Extra-cranial primary malignancy • Neuro-imaging: 1 st line investigation
  • 37.
  • 38. Toxic encephalopathy • Toxic encephalopathy, also known as toxic metabolic encephalopathy, is a degenerative neurologic disorder caused by exposure to toxic substances. • It can be an acute or a chronic disorder. • Toxic encephalopathy can be caused by various chemicals, some of which are commonly used in everyday life (paints, industrial chemicals, and certain metals).
  • 39. EEG in encephalopathy In general, • the most prominent feature of the EEG record in encephalopathies is slowing of the normal background frequency. • Reactivity to photic or other type of external stimulation may be altered. • Some conditions are associated with an increase in seizure frequency, and in such cases, epileptic activity may be recorded.
  • 40. EEG findings • Triphasic has been associated with a wide range of toxic, metabolic, and structural abnormalities. • Triphasic waves are associated with an altered level of consciousness that may range from mild confusion to deep coma. • The background may be slower in hepatic failure • A classic etiology of triphasic wave is hepatic/metabolic encephalopathy. • Triphasic’s are high-amplitude (>70 µV). • Having three phase +ive, -ive and then +ive. • Initial sharp component.
  • 41. Clinical and electrographical features • There is good correlation b/w the severity of the EEG changes , the severity of the encephalopathy and the clinical state of the patient. * • Degree of impairment is clinically categorized as— • *Coma • *Stupourous. • *Lethargy/ hyper-somnia • *Confusion • *Delirium * • Degree of impairment is Electrographically categorized as, • 1.Background slowing without theta delta slow waves. • 2.Diffuse theta delta activity associated with normal background activity. • 3.Slow background activity with diffuse theta delta activity.
  • 42. Clinical and electrographical features & possible pathologies • Background slowing--- cortical (gray matter) dysfunction • Delta theta slow waves – (Brain) white matter disease • Delta theta slow waves , along with slow background activity--- both cortical and white matter disease • Serial EEGs needed to evaluate the course of disease process
  • 43. Grading of EEG abnormalities in diffuse encephalopathy • 1 a --slow background 7-8 Hz without theta delta waves • 1b —4-6 Hz background without theta delta waves • 2a —dominant theta delta with normal background activity. • 2b —dominant theta delta with slow background activity • 3a--dominant delta with normal background activity • 3b—dominant delta with slow background activity • 4a —moderate to high amplitude delta >50 microvolt with no background reactivity • 4b —low amplitude < 5sec • 5a —burst suppression with suppression period < 5sec • 5b —burst suppression with suppression period >5 sec. • 6a —near electro cerebral silence. • 6b --ECS
  • 44. Burst suppression pattern • Recurrent, periodic or pseudo periodic bursts with EEG suppression period of variable duration • Burst can be a mixture of sharp, spike, alpha. theta, delta activities • The suppression period can last from 2s to 20 mint. • Seen in Anoxic brain damage, CNS supressant drugs and severe hypothermia • Paradoxical arousal response • A stimulus brings out slower activity with generalized high voltage delta bursts, that is called as paradoxical arousal response
  • 45. Triphasic waves • Typical and atypical--- * • Typical –initial small negative sharp discharges of 2-4 Hz, followed by large positive sharp discharge and subsequent negative wave. *Frontal dominant, Continuous, stereotyped ,forms a phase lag from anterior to posterior region, seen in hepatic encephalopathy. * • Atypical—less continuous, less stereotyped ,present in uremic, hyperthyroid, toxic encephalopathies • *In dementia (AD) posterior dominant triphasics are present. • TW are also seen in encephalopathies associated with renal failure or electrolyte imbalance, as well as anoxia and intoxications (such as lithium, metrizamide, and levodopa)
  • 46. ECS • *No EEG activity over 2 micro volts when recorded from scalp electrode pairs 10 cm interelectrodes distance. • *Filter settings should not b below 30 Hz and low filter should not be higher than 1 Hz. • *Recording should be at-least one hour, with artifacts free 30 min recording on 2uv. • *Electrodes impedance should be 100ohm to 10Kohm.
  • 47. References • Practical Guide for Clinical Neurophysiologic Testing: EEG: Thoru Yamada MD. • *Basic Principles, Clinical Applications, and Related Fields • *By Ernst Niedermeyer • nelson text book of paediatrics 19th edition
  • 48. Hashimoto’s Encephalopathy • Steroid responsive acute or subacute encephalopathy associated with anti-thyroid antibodies. • Presenting features vary widely. • Psychiatric symptoms around 60%. • TPO and Thyroglobulin. • TSH should be high but patients may be euthyroid or hypothyroid. • Myxedema coma – acute or subacute and precipitated by stress. • Hypothermic, Hypo ventilate, and “suspended animation.”
  • 49. Hyper-Hypoglycemia • Hyperosmolality • Diabetic ketoacidosis – pH doesn’t correlate well with level of consciousness. • Diabetic lactic acidosis. • Sudden lowering of serum osmolality – cerebral edema – can be fatal. • Head trauma and Stroke patients – Glucose control.
  • 50. Hypoglycemia • Stroke like illness. • Delirium. • Coma. • Seizure. Hyperglycemia • Seizures • Hemianopia • Hemichorea/Hemiballismus
  • 51. Hypoglycemic Brain Injury • Range from reversible focal deficits and transient encephalopathy to irreversible coma. • Mean blood glucose was around 30mg/dl. • White matter – more sensitive to ischemia than previously thought. • The duration of hypoglycemia may be difficult to determine in many cases.
  • 52. Hypoxic ischemic encephalopathy • Abnormal neurological behaviour in the neonatal period arising as a result of a hypoxic-ischemic event. • Occurs in1-6 per 1000 term live births in developed countries • 25% die or have multiple disabilities • 4% have mild to moderate forms of cerebral palsy • Essential criteria for diagnosis of HIE: - metabolic acidosis -early onset of encephalopathy -Multisystem organ failure
  • 53.
  • 54. Diagnosis • Mri is the preferred imaging modality in neonates with HIE • CT scan : identifies focal hemorrhagic lesions, diffuse cortical injury and damage to the basal ganglia. • aEEG : determine which infant are at high risk for long term brain injury. Treatment 1.hypothermia 2.Drug therapy : phenobarbital,phenytoin 3. Supportive care
  • 55. WERNICKE ENCEPHALOPATHY • WE is an acute, potentially reversible, neuropsychiatric disorder caused by thiamine deficiency. • The incidence can be as high as 12.5% • The altered cognition of WE can progress to KS, a chronic and usually permanent. • Approximately 80% of patients with acute WE will develop KS. • Mechanism:- Chronic alcoholism – Malnutrition – reduced thiamine uptake and utilization
  • 56. Physical examination • The classical triad of symptoms – only 1/3rd of cases • Ocular abnormalities – nystagmus, bilateral lateral rectus palsies, conjugate gaze palsies, sluggish pupils, ptosis, and anisocoria • Encephalopathy – global confusionalstate, disinterest, inattentiveness, or agitation; Coma is rare. • Gait ataxia – cerebellar damage, and vestibular paresis • Peripheral neuropathy – foot drop, and decreased proprioception
  • 57. Management • Erythrocyte transketolase activity assay, Thiamine assay – very specific tests – not widely available – reserved for diagnostic dilemmas • EEG and CSF analysis may exclude other explanatory or concomitant conditions. • Emergency department care – Parenteral thiamine –Requirement in chronic alcoholics may be as high as 500mg single dose or multiple daily doses. • Never start on Dextrose • Treatment with thiamine repletion, currently recommended at 1 gram of IV thiamine per 24 hours for alcoholics with suspected Wernicke encephalopathy , should not be delayed. • Death occurs in nearly 20 % of patients with delayed treatment. • In-Patient care –Watch for complications – Korsakoff psychosis –Alcohol withdrawal – Congestive heart failure – Lactic acidosis • Out-Patient Care – Thiamine 100 mg PO daily, start alcohol cessation program, Advise on importance of balanced diet.
  • 58. Refrences • Practical Guide for Clinical Neurophysiologic Testing: EEG: Thoru Yamada MD. • Basic Principles, Clinical Applications, and Related Fields • By Ernst Niedermeyer • nelson text book of paediatrics 19th edition